Transport of L-proline was studied with membrane vesicles prepared from the brush borders of the guinea-pig ileum. The presence of an Na+ gradient from outside to inside of the vesicles stimulated L-proline uptake. Accumulation of amino acid in the vesicles reached a maximum 30 s after incubation, then decreased due to efflux and finally equilibrated at a level nearly identical to that shown in the absence of an Na+ gradient in 30 min. The peak level of the uptake was 3.5-times greater than the final equilibrium level. The equilibrium level of L-proline uptake decreased with increasing medium osmolarity. Extrapolation to infinite medium osmolarity, that is, under the condition of zero intravesicular space, showed no uptake, indicating transport of L-proline into membrane vesicles. The initial rate of uptake for 15 s was enhanced with increasing concentrations of Na+ in the external medium. A small part of the L-proline transport occurred by simple diffusion in addition to Na+-gradient-dependent transport. When L-proline concentrations were varied and transport due to diffusion was subtracted, the initial rate of uptake dependent on Na+ gradient (out greater than in) obeyed Michaelis-Menten kinetics with Km and V values of 0.67 mM and 2.73 nmol/15 s per mg protein, respectively. Evidence was obtained which indicates that L-cysteine is a substract specific for transport through system ASC (alanine-, serine-, and cysteine-preferring) and that transport in the presence of an Li+ gradient (out > in) also takes palce by the ASC system. The uptake of L-proline in the presence of an Na+ gradient (out > in) was inhibited 90% by a large excess of alpha-(methylamino)-isobutyrate, the model substrate specific for the A system (alanine-preferring). This indicates than 90% of Na+-gradient-dependent L-proline uptake is supported by the A system. The remaining 10% of L-proline uptake was found to be catalyzed by the ASC system, since L-proline uptake equivalent to this alpha-(methylamino)-isobutyrate-uninhibited part was demonstrated in the presence of Li+ gradient.

Aminoisobutyric Acids↗

PubMed1980

Block of acid secretion by amytal and its partial reversal by menadione with ascorbate in the gastric mucosa of the guinea-pig.

The effect of amytal on energy metabolism and acid secretion in an isolated gastric mucosa of the guinea-pig were studied. Determination of adenine nucleotides, creatine phosphate, pyruvate and lactate in the gastric mucosa showed that amytal depressed the levels of ATP, creatine phosphate and energy charge with elevation of the AMP and pyruvate levels. This treatment inhibited concomitantly acid secretion and active chloride transport detected by short circuit current. The addition of menadione with ascorbate to the medium in the presence of amytal partially restored ATP and energy charge levels and also induced a partial recovery of acid secretion and activ chloride transport. These results suggest that ATP is a direct energy donor for acid secretion in the gastric mucosa of the guinea-pig.

Adenine Nucleotides↗

PubMed1980

[Endocrine interrelationship between the pancreas and digestive system].

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Adenoma, Islet Cell↗

PubMed1980

Increase in pepsin content in gastric mucosa during the course of aspirin- and taurocholate-induced gastric ulceration in rats.

To investigate the possible role of pepsin in ulceration induced by hydrogen ion back-diffusion, the ratio of alkali-labile pepsinogen to total pepsinogen was studied during the course of aspirin- and taurocholate-induced gastric ulceration in comparison with the changes in the ion permeability and histological findings. The results obtained were as follows. (1) The increase in the ulcer index was observed between 1 and 2 hr with intragastric aspirin and between 2 and 4 hr with intragastric taurocholate. (2) The back-diffusion of luminal hydrogen ions, observed as a significant decrease in hydrogen ion net flux, occurred immediately in both cases with aspirin and with taurocholate. (3) A significant increase in the ratio of alkali-labile to total pepsinogen in the homogenate of gastric mucosa was observed at 30 min with aspirin and at 60 min with taurocholate. (4) Histological examination revealed the degeneration of mucosal cells spreading from the luminal surface into the mucosa, which fell off after 120 min with aspirin. These findings indicate that the activated pepsin is involved in the ulcer formation caused by the hydrogen ion back-diffusion, although the origin of the activated pepsin is not clear at the present time.

Animals↗

PubMed1980

The increase in cyclic AMP content in the isolated guinea pig gastric mucosa during histamine-stimulated acid secretion.

Using the isolated guinea pig gastric mucosa perfused in vitro with a constant acid secretion and potential difference, the cyclic AMP (cAMP) contents in the gastric mucosa and in the serosal solution were measured during the course of acid secretion stimulated by histamine or dibutyryl cyclic AMP (db-cAMP). (1) The acid-secreting response of the gastric mucosa to histamine was reproduced by addition of db-cAMP. (2) The acid secretion stimulated by db-cAMP was not inhibited. (3) The increase in mucosal cAMP content was accompanied by histamine-stimulated acid secretion. (4) The increase in the mucosal cAMP content preceded the increase in acid secretion stimulated by histamine. From these findings, it has been concluded that cAMP plays an important role in the mechanism of histamine-stimulated acid secretion, including the morphological transformation of parietal cells, although its role as the intracellular mediator of the stimuli for the hydrogen ion pump itself requires further investigation.

Animals↗

PubMed1980

Aspirin- and taurocholate-induced metabolic damage in mammalian gastric mucosa in vitro.

To clarify the mechanism of initiation of the hydrogen ion backdiffusion, the effects of aspirin and taurocholate, two representative gastric mucosal barrier breakers, on the potential difference, secretory activity, energy metabolism, and the hydrogen ion permeability of guinea pig gastric mucosa was studied in vitro. 1) The ATP content and energy charge of the gastric mucosa showed a statistically significant reduction when the potential difference decreased to one-half of that before addition. 2) The mucosal acid secretion was reduced by addition of the barrier breaker. 3) However, the hydrogen ion backdiffusion, as measured by titrating the acid appearing in the serosal solution, became detectable when the potential difference decreased to one-fourth of that before addition. It has been concluded, therefore, that the primary action of gastric mucosal barrier breakers is to damage the energy metabolism of the mucosal cells, and that the hydrogen ion backdiffusion takes place as the result of cellular death caused by the impairment of energy metabolism.

Adenosine Diphosphate↗